63Shortness of Breath
Answers
46.The answer is d.(Mycek et al, p 187.)The patient has angioedema, a
rare, but significant side effect of angiotensin-converting enzyme (ACE-I)
inhibitors. This type of angioedema is usually limited to the lips, tongue,
and face. If pharyngeal or laryngeal structures become involved, or there is
significant tongue swelling, the patient may begin to compromise their
airwayand emergent intubation or surgical cricothyroidotomy needs to be
performed. ACE-I–induced angioedema can occur after short- or long-
term use of the medication. None of the other medications listed cause
angioedema. The medication should be immediately discontinued.
47.The answer is a.(Rosen, pp 1226-1228.)The patient has a confirmed
venous thrombosis and has symptoms consistent with a pulmonary throm-
boembolism. Data now show that almost every deep venous thrombosis
(DVT) embolizes to some extent. The presence of a PE in this patient can be
presumed by a confirmed DVT with pulmonary symptoms. All patients
need to be on a monitor and should receive supplemental oxygen despite
normal oxygen saturation. Oxygen acts as a pulmonary vasodilator. Heparin
is the first-line therapy in this patient and should be administered promptly.
Failure to achieve a therapeutic partial thromboplastin time (PTT) value
within the first 24 hours leads to a 23% incidence of new embolism.
(b)A chest CT scan is not urgently needed since a DVT is already con-
firmed by duplex ultrasound and should not delay administration of antico-
agulation.(c)Aspirin is not effective in preventing propagation of a DVT. The
patient requires an anticoagulant, not an antiplatelet agent. (d)Although
immobility can lead to increased thrombus, a patient with a diagnosed DVT
should be monitored in bed while receiving anticoagulation. (e)Warfarin
should never be started without concomitant administration of heparin. After
the international normalized ratio (INR) is at a therapeutic level (2-3 IU),
heparin can be stopped and warfarin can be taken alone. Warfarin initially
causes a temporary hypercoagulable state because the anticoagulants, protein
C and S (inhibited by warfarin), have shorter half-lives compared with the
procoagulant vitamin K–dependent proteins that warfarin also inhibits.